NLE Renal & Urinary Nursing — Acute & Chronic Kidney DiseaseRevision Notes

Formulas

Exam Tips

• NLE FAVORITE: Which phase of AKI is most dangerous? → OLIGURIC phase (hyperkalemia + fluid overload).
• If the question asks about a patient who just recovered from AKI and now has 4 L/day urine output with weakness and leg cramps — think DIURETIC phase with HYPOKALEMIA.
• Prerenal clue words in NLE stems: 'after hemorrhage,' 'severe dehydration,' 'cardiogenic shock,' 'third-degree burns,' 'sepsis.' BUN:Creatinine >20:1.
• Intrarenal clue words: 'received gentamicin for 2 weeks,' 'IV contrast for CT scan,' 'NSAID use for months.' BUN:Creatinine ~10:1.
• Postrenal clue: 'elderly male with difficulty urinating,' 'ureteral stone,' 'pelvic tumor.' → Relieve obstruction.

Key Points

• AKI is a SUDDEN and often REVERSIBLE decline in kidney function, characterized by rising BUN and creatinine and usually decreased urine output (oliguria).
• THREE CAUSES by location: Prerenal (poor perfusion — most common), Intrarenal/Intrinsic (direct kidney damage — ATN is the top example), Postrenal (obstruction — BPH, stones).
• Prerenal BUN:Creatinine ratio is >20:1 because urea is reabsorbed in a low-flow state; intrarenal ratio is approximately 10:1 because the tubules are damaged and cannot reabsorb properly.
• FOUR PHASES: Onset → Oliguric → Diuretic → Recovery (Convalescent).
• OLIGURIC PHASE (<400 mL/day, lasting 1–3 weeks) is the MOST DANGEROUS — hyperkalemia, fluid overload, metabolic acidosis, and uremia accumulate rapidly.
• DIURETIC PHASE: urine output rises to 3–5 L/day but tubules cannot yet concentrate urine — risk of DEHYDRATION, HYPOKALEMIA, and HYPONATREMIA (fluid/electrolyte LOSS, opposite of oliguric phase).
• Recovery phase may take weeks to months; some nephron deficit may be permanent.
• Nephrotoxic causes of intrarenal AKI include aminoglycoside antibiotics (gentamicin, amikacin), IV contrast dye, NSAIDs — important drug safety issue in Philippine clinical settings.
• ATN (Acute Tubular Necrosis) from ischemia or nephrotoxins is the most common cause of intrarenal AKI.

Definitions

Section Title

Acute Kidney Injury (AKI): Pathophysiology, Causes, and Phases

Common Mistakes

• Confusing the DIURETIC phase with recovery — the patient is still very sick during diuresis; electrolyte loss (hypokalemia, hyponatremia) is now the danger, not retention.
• Forgetting that BUN elevation alone is not specific for kidney disease — it also rises with GI bleeding, high protein intake, or corticosteroid use. Use BUN:Creatinine ratio in context.
• Giving nephrotoxic medications (NSAIDs, aminoglycosides) without checking renal function or adjusting dose — a major nursing accountability issue under RA 9173.
• Assuming oliguria always means AKI — also assess for catheter obstruction (kinked tubing) before concluding decreased output is pathologic.
• Mixing up fluid management: during OLIGURIC phase → restrict fluids; during DIURETIC phase → replenish fluids and electrolytes.

Exam Tips

• NLE STEM: 'Patient with AKI has peaked T waves on ECG. What is the PRIORITY nursing action?' → Prepare and administer IV Calcium Gluconate (protect heart FIRST).
• Remember the sequence: PROTECT (Ca Gluconate) → SHIFT (Insulin/Dextrose, NaHCO3) → REMOVE (Kayexalate, Dialysis).
• Albuterol (nebulized) also shifts K⁺ into cells — useful when IV access is difficult or as adjunct.
• The NLE often tests the SEQUENCE of interventions — know which acts fastest and why each is used.
• If a question asks 'which food should the renal patient avoid?' — choose the high-potassium option (banana, orange, potato, tomato).

Key Points

• HYPERKALEMIA (serum K⁺ >5.5 mEq/L) is the most immediately life-threatening complication of both AKI and CKD — causes fatal cardiac arrhythmias.
• ECG CHANGES in sequence (low to high K⁺): Peaked (tall, narrow, tent-shaped) T waves → Prolonged PR interval → Widened QRS → Sine wave pattern → Ventricular fibrillation/asystole.
• EMERGENCY MANAGEMENT follows a logical three-step sequence: (1) PROTECT the heart, (2) SHIFT K⁺ into cells, (3) REMOVE K⁺ from the body.
• Step 1 — PROTECT: IV Calcium Gluconate — stabilizes cardiac membrane; acts in MINUTES; does NOT lower serum K⁺ level but prevents arrhythmia while other treatments work.
• Step 2 — SHIFT K⁺ INTO CELLS: IV Regular Insulin + Dextrose 50% (insulin drives K⁺ into cells; dextrose prevents hypoglycemia); IV Sodium Bicarbonate (alkalinizes blood → H⁺ leaves cells, K⁺ enters); Nebulized Albuterol/Beta-agonists.
• Step 3 — REMOVE K⁺: Sodium Polystyrene Sulfonate (Kayexalate) — ion-exchange resin given orally or per rectum; Dialysis — most effective and fastest removal method.
• Dietary restriction: avoid high-potassium foods — bananas, oranges, tomatoes, potatoes, dried fruits, nuts, dark leafy vegetables (abundant in Filipino diet, e.g., kamote tops, malunggay, saging).
• Teach patient to read food labels and avoid salt substitutes (contain potassium chloride instead of sodium chloride).

Definitions

Section Title

Hyperkalemia: The #1 Life Threat in Renal Failure

Common Mistakes

• Giving Kayexalate FIRST in a patient with ECG changes from hyperkalemia — WRONG. IV Calcium Gluconate must come FIRST to protect the heart.
• Forgetting that Insulin + Dextrose only SHIFTS potassium (temporary) — it does NOT remove potassium from the body.
• Confusing Calcium Gluconate (for hyperkalemia/cardiac membrane stabilization) with Calcium Chloride — both are calcium salts but differ in concentration and clinical use.
• Not monitoring blood glucose after insulin administration for hyperkalemia — hypoglycemia is a real risk.
• Advising renal patients that 'natural' fruit juices or herbal teas are safe — many are very high in potassium.

Formulas

Exam Tips

• CKD vs. AKI distinction: CKD = progressive + irreversible + bilateral small shrunken kidneys on ultrasound. AKI = sudden + potentially reversible + normal or enlarged kidneys.
• NLE FREQUENTLY TESTED: Why does CKD cause hypocalcemia? → Damaged kidneys cannot convert Vitamin D to calcitriol → less calcium absorbed from gut.
• Why does CKD cause anemia? → Damaged kidneys produce less erythropoietin → fewer RBCs.
• DRUGS TO AVOID in CKD: NSAIDs, magnesium antacids, nephrotoxic antibiotics (aminoglycosides), and renally cleared drugs without dose adjustment.
• ACE Inhibitors (enalapril, captopril) and ARBs (losartan) → renoprotective BUT watch for hyperkalemia and rising creatinine.

Key Points

• CKD is PROGRESSIVE and IRREVERSIBLE loss of nephrons over months to years — unlike AKI which is potentially reversible.
• Staged by GFR (Glomerular Filtration Rate): Stage 1 (GFR ≥90, kidney damage with normal GFR) → Stage 2 (60–89) → Stage 3 (30–59) → Stage 4 (15–29) → Stage 5/ESRD (GFR <15 mL/min).
• LEADING CAUSES in the Philippines and globally: DIABETES MELLITUS (#1) and HYPERTENSION (#2).
• UREMIA: the systemic toxic syndrome from retained metabolic wastes — affects virtually every body system.
• ANEMIA in CKD: caused by reduced erythropoietin production by damaged kidneys → fewer RBCs → fatigue, pallor, dyspnea. Treated with Erythropoiesis-Stimulating Agents (ESA) like Epoetin Alfa + iron supplementation.
• CALCIUM-PHOSPHATE IMBALANCE: damaged kidneys cannot activate Vitamin D (to calcitriol) → decreased GI calcium absorption + kidneys cannot excrete phosphate → HYPOCALCEMIA + HYPERPHOSPHATEMIA → secondary hyperparathyroidism → bone resorption → RENAL OSTEODYSTROPHY.
• CARDIOVASCULAR complications (hypertension, heart failure, pericarditis) are the LEADING CAUSE OF DEATH in CKD/ESRD patients.
• UREMIC FROST: white crystalline deposits of urea on the skin — a sign of very severe, advanced uremia.
• UREMIC FETOR: ammonia-like smell on the breath from urea being converted to ammonia by oral bacteria.
• METABOLIC ACIDOSIS is chronic in CKD because kidneys cannot excrete H⁺ or regenerate HCO₃⁻.
• ACE Inhibitors and ARBs slow CKD progression (reduce intraglomerular pressure) but require monitoring of potassium (can worsen hyperkalemia) and creatinine.

Definitions

Section Title

Chronic Kidney Disease (CKD) and ESRD: Multisystem Impact

Common Mistakes

• Giving magnesium-containing antacids (e.g., Milk of Magnesia, Maalox) to CKD patients — kidneys cannot excrete magnesium → hypermagnesemia → CNS and cardiac depression.
• Giving NSAIDs for pain in CKD patients — NSAIDs reduce renal prostaglandins → worsen renal perfusion → accelerate CKD progression.
• Teaching patients to take phosphate binders on an empty stomach — they MUST be taken WITH meals to bind dietary phosphate.
• Confusing the anemia of CKD (normocytic, from low erythropoietin) with iron-deficiency anemia (microcytic) — both may coexist; iron supplementation is needed alongside ESA.
• Forgetting that protein restriction applies PRE-DIALYSIS — once on dialysis, protein intake is often INCREASED because dialysis removes amino acids.

Exam Tips

• NLE CLASSIC: 'How do you assess AV fistula patency?' → PALPATE for THRILL and AUSCULTATE for BRUIT.
• 'What should the nurse do if no thrill/bruit is detected?' → Report to physician IMMEDIATELY (possible thrombosis — time-sensitive emergency).
• The most COMMON complication of HD = HYPOTENSION (from rapid fluid removal).
• Disequilibrium syndrome is more common in FIRST FEW SESSIONS of HD — slow the dialysis rate as prevention.
• Remember: 4 NONOs for fistula arm — No BP, No IV, No blood draw, No tight items.

Key Points

• HD filters blood through an external dialyzer machine — typically 3–4 hours per session, 3 times per week.
• VASCULAR ACCESS options (in order of preference): AV Fistula (preferred — lowest infection/clotting risk, needs 6–12 weeks to mature) → AV Graft (synthetic tube; matures faster but higher infection/clot risk) → Central Venous Catheter/Permcath (temporary; highest infection risk).
• AV FISTULA ASSESSMENT is a TOP NLE priority: Palpate for THRILL (buzzing vibration = blood flowing = patent) and Auscultate for BRUIT (whooshing sound = patent). ABSENCE of thrill or bruit = possible clotting → report IMMEDIATELY.
• AV FISTULA ARM PROTECTION (4 NONOs): NO blood pressure measurement, NO venipuncture/blood draws, NO IV lines, NO tight clothing or jewelry on the access arm.
• Additional fistula care: do NOT sleep on the access arm; report any redness, swelling, warmth (signs of infection) or loss of thrill/bruit.
• WEIGH patient BEFORE and AFTER dialysis — weight difference = fluid removed during session (goal is to achieve 'dry weight').
• HD COMPLICATIONS to monitor: Hypotension (most common during HD — from rapid fluid removal), Disequilibrium Syndrome (rapid solute shifts → cerebral edema → headache/seizures — more common in new patients), Bleeding (heparin is used during HD to prevent clotting in the dialyzer), Air Embolism (rare but fatal), Infection.
• Hold DIALYZABLE medications until AFTER HD (many antihypertensives, some antibiotics — check with pharmacist; otherwise drug is removed during dialysis and patient gets no therapeutic benefit).
• HEPARIN is used during HD to prevent clotting in the dialyzer circuit — monitor for post-dialysis bleeding at access site and systemically.

Definitions

Section Title

Hemodialysis (HD): Access Care and Nursing Management

Common Mistakes

• Taking blood pressure on the AV fistula arm — even routine BP cuffs can compress the fistula and cause thrombosis.
• Not checking for thrill/bruit before, during, and after HD — a clotted fistula is an emergency that requires immediate reporting.
• Giving all medications at the scheduled time regardless of dialysis schedule — dialyzable drugs given before HD may be completely removed by dialysis.
• Interpreting post-HD weight GAIN as the patient eating more — it usually means inadequate fluid removal during the session.
• Forgetting that heparin used during HD increases bleeding risk — check access site for prolonged bleeding after needle removal.

Exam Tips

• NLE FAVORITE: 'PD outflow is cloudy. What is the PRIORITY action?' → Report to physician IMMEDIATELY and send specimen for culture — suspected PERITONITIS.
• 'PD outflow is less than inflow. What should the nurse do FIRST?' → REPOSITION the patient (turn, ambulate); check for catheter kinks.
• Remember: WARM dialysate before instilling — cold causes pain AND reduces efficiency.
• PD is GENTLER than HD — better for hemodynamically unstable patients, diabetics, children, and those who prefer home therapy.
• Teach patient: strict hand hygiene and aseptic technique is the #1 prevention for peritonitis.

Key Points

• PD uses the patient's own PERITONEAL MEMBRANE as the dialysis filter — no machine needed for the actual filtration.
• CYCLE: FILL (instill warmed dialysate into peritoneal cavity via catheter) → DWELL (dialysate stays; diffusion and osmosis remove wastes/fluid from blood into dialysate) → DRAIN (drain spent dialysate out — called 'effluent').
• WARM the dialysate to body temperature (37°C) BEFORE instilling — cold dialysate causes abdominal cramping, pain, and vasoconstriction of peritoneal vessels reducing efficiency.
• NORMAL outflow (effluent) = clear and pale yellow in color.
• CLOUDY/TURBID outflow = PERITONITIS — the most serious and most common major complication of PD. Also assess for fever, abdominal pain, and rebound tenderness.
• STRICT ASEPTIC TECHNIQUE at every connection, disconnection, and catheter care to prevent peritonitis.
• If OUTFLOW IS LESS THAN INFLOW (poor drainage): Turn/reposition the patient (especially left lateral or standing), check for catheter kinks, ensure drainage bag is below the level of the abdomen (gravity). Persistent positive balance = fluid retention = hypertonic solution may be needed.
• Types of PD: CAPD (Continuous Ambulatory PD — manual exchanges ~4 times/day) and CCPD/APD (Continuous Cycling PD — automated machine at night).
• ADVANTAGES of PD over HD: gentler and more continuous (better hemodynamic stability), can be done at home, fewer fluid and diet restrictions, no need for vascular access.
• DISADVANTAGES of PD: risk of peritonitis, catheter-related infections, protein loss through peritoneal membrane, not suitable for patients with abdominal adhesions or recent abdominal surgery.
• Dextrose concentration in dialysate: higher glucose concentration = greater osmotic pull = more fluid removal. Used for fluid overloaded patients.

Definitions

Section Title

Peritoneal Dialysis (PD): Technique and Complications

Common Mistakes

• Instilling COLD dialysate directly from refrigerator storage — always warm to body temperature first using a dry warming pad (NOT microwave, which creates hot spots).
• Ignoring slightly cloudy outflow and attributing it to fibrin — any cloudiness must be assessed as peritonitis until proven otherwise.
• Using contaminated or non-sterile technique at connections — even brief breaks in aseptic technique can cause peritonitis.
• Not repositioning the patient when outflow is poor — lying supine can cause the catheter to be obstructed by loops of bowel; repositioning is the FIRST intervention.
• Confusing hypertonic and isotonic dialysate use — hypertonic (higher dextrose) is for fluid overloaded patients; using it unnecessarily risks dehydration.

Exam Tips

• POST-TRANSPLANT PRIORITY: Monitor URINE OUTPUT HOURLY. If it drops → suspect rejection → report immediately.
• Signs of rejection mnemonic: FODUP — Fever, Oliguria, Decreased urine output, Uremia rising (creatinine), Pain over graft.
• NEVER miss immunosuppressant doses → risk of rejection. Teach patient this is a LIFELONG commitment.
• Immunosuppression → HIGH infection risk → teach meticulous infection prevention (handwashing, avoid sick contacts, promptly report fever).
• NLE may ask about GRAFT LOCATION — it is in the ILIAC FOSSA (pelvis), not the flank.

Key Points

• Kidney transplant is the DEFINITIVE treatment for ESRD — better quality of life and survival than dialysis.
• Donor kidney is placed in the ILIAC FOSSA (right or left lower quadrant) — NOT where the native kidneys are. Native kidneys are usually LEFT IN PLACE unless causing problems.
• POST-OP PRIORITY #1: Monitor URINE OUTPUT HOURLY — this directly reflects graft function. Expect large urine output initially (the new kidney filters the accumulated fluid/solutes). Decreasing urine output may signal rejection or a surgical complication.
• LIFELONG IMMUNOSUPPRESSION is required to prevent rejection — regimens typically include a calcineurin inhibitor (Cyclosporine or Tacrolimus), a corticosteroid (Prednisone), and an antiproliferative agent (Mycophenolate Mofetil/CellCept).
• The great trade-off: immunosuppression prevents rejection but creates HIGH SUSCEPTIBILITY TO INFECTION — infection is a leading cause of death post-transplant.
• SIGNS OF ACUTE REJECTION: Decreased urine output (oliguria), Fever, Pain/tenderness over the graft site (iliac fossa), Rising serum creatinine, Weight gain, Hypertension. Report IMMEDIATELY.
• TYPES OF REJECTION: Hyperacute (within minutes to hours — irreversible, graft must be removed), Acute (days to months — treatable with high-dose steroids, OKT3), Chronic (months to years — gradual decline, less treatable).
• INFECTION PREVENTION post-transplant: avoid crowds and sick contacts, practice strict hand hygiene, report fever >38°C immediately, take prophylactic antivirals/antifungals as prescribed.
• MEDICATION ADHERENCE: NEVER miss immunosuppressant doses — even one missed dose can trigger rejection. Teach patient to take drugs at the same time daily.
• Monitor for drug toxicity: Cyclosporine → nephrotoxicity and hypertension; Tacrolimus → nephrotoxicity, neurotoxicity, hyperglycemia; Corticosteroids → Cushing's syndrome, hyperglycemia, osteoporosis.

Definitions

Section Title

Kidney Transplant: Post-op Care and Rejection

Common Mistakes

• Forgetting to monitor urine output HOURLY post-transplant — this is the most critical parameter for graft function and must not be overlooked.
• Teaching patient that 'feeling better' means they can reduce immunosuppressant doses — NEVER. Immunosuppression must continue for life regardless of how well the patient feels.
• Attributing fever to normal post-op response — in an immunosuppressed transplant patient, fever = infection until proven otherwise. Report immediately.
• Not recognizing signs of rejection — graft tenderness is often subtle (the new kidney is in the pelvis, not where the original kidneys are).
• Confusing the graft location — transplanted kidney is in the ILIAC FOSSA (right lower abdomen for right kidney, left for left), not in the flank like native kidneys.

Formulas

Exam Tips

• Post-TURP drainage expected → PINK and gradually clearing. BRIGHT RED with clots = hemorrhage → SPEED UP irrigation, call physician.
• NLE FORMULA: True Urine = Total Drainage MINUS Irrigation instilled. Practice this calculation.
• Tamsulosin (Flomax) → orthostatic hypotension → teach patient to SIT on bedside first before standing.
• Finasteride = TERATOGENIC → pregnant women MUST NOT HANDLE crushed tablets.
• TUR Syndrome signs: confusion + low sodium (dilutional hyponatremia) after TURP → emergency.

Key Points

• BPH = non-malignant (benign) enlargement of the prostate gland in aging men (most common in men >50 years).
• Enlarged prostate compresses the urethra → BLADDER OUTLET OBSTRUCTION → LUTS (Lower Urinary Tract Symptoms).
• BPH is a POSTRENAL cause of urinary obstruction — if untreated, can cause hydronephrosis and kidney damage.
• LUTS of BPH (two groups): OBSTRUCTIVE symptoms (hesitancy, weak/intermittent stream, straining, incomplete emptying, urinary retention) and IRRITATIVE/STORAGE symptoms (frequency, urgency, nocturia, dysuria).
• DIGITAL RECTAL EXAM (DRE): prostate feels smooth, firm, symmetrically enlarged (NOT hard/nodular — that raises concern for cancer/malignancy).
• PSA (Prostate-Specific Antigen) may be mildly elevated in BPH but very elevated PSA suggests prostate CANCER.
• PHARMACOLOGY: Alpha-1 Blockers (tamsulosin/Flomax, terazosin, doxazosin) → relax smooth muscle of prostate and bladder neck → improve urine flow within days. MAJOR SIDE EFFECT: ORTHOSTATIC HYPOTENSION — teach patient to rise slowly from lying/sitting position, especially after first dose.
• 5-Alpha-Reductase Inhibitors (Finasteride/Proscar, Dutasteride) → reduce prostate size by blocking DHT conversion. Takes 3–6 months for effect. IMPORTANT: TERATOGENIC — pregnant women must NOT handle crushed or broken tablets (risk of fetal male genital abnormalities).
• SURGERY: TURP (Transurethral Resection of the Prostate) — most common surgical procedure for BPH.
• POST-TURP: Continuous Bladder Irrigation (CBI) with normal saline is maintained to prevent blood clot obstruction of the catheter.
• CBI ASSESSMENT: Expected drainage = PINK to light-red and gradually clearing over 24–48 hours. ABNORMAL = bright-red drainage, thick like ketchup, with large clots = HEMORRHAGE → speed up irrigation rate to flush clots out AND notify physician.
• TRUE URINE OUTPUT CALCULATION with CBI: True Urine Output = Total Drainage Output MINUS Total Irrigation Fluid Instilled.
• TUR SYNDROME: absorption of large amounts of irrigating fluid through open prostatic veins → dilutional hyponatremia → confusion, bradycardia, hypertension, visual changes. EMERGENCY.
• Retrograde ejaculation is a common post-TURP complication — semen goes backward into bladder instead of out — counsel patient about this (fertility affected, but not sexual function).

Definitions

Section Title

Benign Prostatic Hyperplasia (BPH) and Post-TURP Care

Common Mistakes

• Forgetting to subtract irrigation fluid when calculating urine output post-TURP — reporting 'high urine output' when it is mostly irrigation fluid is a significant clinical error.
• Slowing down CBI when drainage becomes bright red — WRONG. Speed up the irrigation to flush out clots and call the physician (hemorrhage).
• Teaching a patient on tamsulosin to take the drug and stand up quickly afterward — orthostatic hypotension is the #1 safety concern; always instruct to rise SLOWLY.
• Crushing finasteride tablets to make them easier to swallow in the presence of a pregnant caregiver — teratogenic risk; intact tablets should be handled only by non-pregnant individuals.
• Confusing BPH with prostate cancer on exam questions — BPH: smooth, rubbery, symmetrically enlarged; prostate CA: hard, nodular, asymmetric on DRE.